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548 results for “DNA repair”
An Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies
ClinicalTrials.gov study NCT02854436. IPD Sharing: Not stated. Countries: 15. Publications: 2.
Trial of Rucaparib in Patients With Metastatic Hormone-Sensitive Prostate Cancer Harboring Germline DNA Repair Gene Mutations
ClinicalTrials.gov study NCT03413995. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Microscopy data from: Identification of genetic interactions with priB links the PriA/PriB DNA replication restart pathway to double-strand DNA break repair in Escherichia coli
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Data from: Evidence of centromeric histone 3 chaperone involved in DNA damage repair pathway in budding yeast
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Data from: Tissue-specific mutagenesis from endogenous guanine damage is suppressed by PolK and DNA repair
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Data from: Gal-1 promotes lung cancer cell survival by enhancing PARP1/H1.2 interaction to promote DNA repair upon DNA damage response
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Recurrent mismatch binding by MutS mobile clamps on DNA localizes repair complexes nearby
<p>DNA mismatch repair (MMR), the guardian of the genome, commences when MutS identifies a mismatch and recruits MutL to nick the error-containing strand, allowing excision and DNA resynthesis. Dominant MMR models posit that after mismatch recognition, ATP converts MutS to a hydrolysis-independent, diffusive mobile clamp that no longer recognizes the mismatch. Little is known about the postrecognition MutS mobile clamp and its interactions with MutL. Two disparate frameworks have been proposed: One in which MutS–MutL complexes remain mobile on the DNA, and one in which MutL stops MutS movement. Here we use single-molecule FRET to follow the postrecognition states of MutS and the impact of MutL on its properties. In contrast to current thinking, we find that after the initial mobile clamp formation event, MutS undergoes frequent cycles of mismatch rebinding and mobile clamp reformation without releasing DNA. Notably, ATP hydrolysis is required to alter the conformation of MutS such that it can recognize the mismatch again instead of bypassing it; thus, ATP hydrolysis licenses the MutS mobile clamp to rebind the mismatch. Moreover, interaction with MutL can both trap MutS at the mismatch en route to mobile clamp formation and stop movement of the mobile clamp on DNA. MutS's frequent rebinding of the mismatch, which increases its residence time in the vicinity of the mismatch, coupled with MutL's ability to trap MutS, should increase the probability that MutS–MutL MMR initiation complexes localize near the mismatch.</p> <p> </p>
Data from: Topological DNA-binding of SMC-like RecN promotes RecA-mediated DNA double-strand break repair
<p>Bacterial RecN, closely related to the structural maintenance of chromosomes (SMC) family of proteins, functions in the repair of DNA double-strand breaks (DSBs) by homologous recombination. However, the understanding of how RecN acts in concert with the RecA recombinase to promote DSB repair remains limited. Here, we demonstrated that the purified Escherichia coli RecN protein topologically loads onto both single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) that has a preference for ssDNA. RecN topologically bound to dsDNA slides off the end of linear dsDNA, but this is prevented by RecA nucleoprotein filaments on ssDNA, thereby allowing RecN to translocate to DSBs. Furthermore, we found that, once RecN is recruited onto ssDNA, it can topologically capture a second dsDNA substrate in an ATP-dependent manner, suggesting a role in synapsis. Indeed, RecN stimulates RecA-mediated D-loop formation and subsequent strand exchange activities. Our findings provide mechanistic insights into the recruitment of RecN to DSBs and sister chromatid interactions by RecN, both of which function in RecA-mediated DSB repair.</p>
Data from: Long term effects of superoxide and DNA repair on lizard telomeres
Telomeres are the non-coding protein-nucleotide 'caps' at chromosome ends that contribute to chromosomal stability by protecting the coding parts of the linear DNA from shortening at cell division, and from erosion by reactive molecules. Recently, there has been some controversy between molecular and cell biologists, on the one hand, and evolutionary ecologists on the other, regarding whether reactive molecules erode telomeres during oxidative stress. Many studies of biochemistry and medicine have verified these relationships in cell culture, but other researchers have failed to find such effects in free-living vertebrates. Here we use a novel approach to measure free radicals (superoxide), mitochondrial 'content' (a combined measure of mitochondrial number and size in cells), telomere length and DNA damage at two primary time points during the mating season of an annual lizard species (Ctenophorus pictus). Superoxide levels early in the mating season vary widely and elevated levels predict shorter telomeres both at that time as well as several months later. These effects are likely driven by mitochondrial content, which significantly impacts late season superoxide (cells with more mitochondria have more superoxide), but superoxide effects on telomeres are counteracted by DNA repair as revealed by 8-hydroxy-2'-deoxyguanosine assays. We conclude that reactive oxygen species and DNA repair are fundamental for both short- and long-term regulation of lizard telomere length with pronounced effects of early-season cellular stress detectable on telomere length near lizard death.
NGS data from: Predominant HDR-dependent genome editing and prevention of byproducts by DNA repair pathway choice
<p>CRISPR-Cas9 genome editing has been widely adapted to cleave genomic DNA sequences of interest. Cellular repair of the CRISPR induced DNA double-strand breaks is dominated by error prone end joining pathways that outcompete inefficient homology-directed repair (HDR) that would allow precise introduction of a mutation present in a supplied synthetic DNA donor. To achieve predominant HDR, we studied the combinatory effect of inhibitory mutations in genes that are central to competing repair pathways.</p>
Analysis of Androgene Receptors Axis and DNA Damage Repair Genes in Patients With Prostate Cancer
ClinicalTrials.gov study NCT03677414. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Naproxen in Preventing DNA Mismatch Repair Deficient Colorectal Cancer in Patients With Lynch Syndrome
ClinicalTrials.gov study NCT02052908. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Abiraterone/Prednisone, Olaparib, or Abiraterone/Prednisone + Olaparib in Patients With Metastatic Castration-Resistant Prostate Cancer With DNA Repair Defects
ClinicalTrials.gov study NCT03012321. IPD Sharing: Not stated. Countries: 1. Publications: 1.
AsiDNA (a DNA Repair Inhibitor) Administered IntraVenously in Advanced Solid Tumors
ClinicalTrials.gov study NCT03579628. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Chlorambucil in Metastatic PDAC Patients Bearing a Germ Line DNA Defects Repair Mutations (SALE Trial)
ClinicalTrials.gov study NCT04692740. IPD Sharing: NO. Countries: 1. Publications: 5.
Examination of Clinical and Laboratory Abnormalities in Patients With Defective DNA Repair: Xeroderma Pigmentosum, Cockayne Syndrome, or Trichothiodystrophy
ClinicalTrials.gov study NCT00001813. IPD Sharing: YES. Countries: 1. Publications: 4.
DNA Damage & Repair Proteins In Patients With Atherosclerotic Coronary Artery Disease
ClinicalTrials.gov study NCT02335086. IPD Sharing: Not stated. Countries: 1. Publications: 2.
A Phase II Study of Nivolumab in Patients With Genetic Alterations in DNA Damage Repair and Response Who Progressed After Standard Treatment for Metastatic Solid Cancers
ClinicalTrials.gov study NCT04761744. IPD Sharing: NO. Countries: 1. Publications: 33.
Quantification of DNA Repair Products in the Urine After Ultraviolet Radiation of the Skin
ClinicalTrials.gov study NCT05277961. IPD Sharing: NO. Countries: 1. Publications: 4.
Actinic Cheilitis Pre-Treated With DNA Repair Enzyme Cream
ClinicalTrials.gov study NCT03224715. IPD Sharing: NO. Countries: 1. Publications: 4.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.